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Monday, November 25, 2013

B-vitamins, brain shrinkage and Alzheimer's disease

Globally, we are approaching a diagnostic rate for
Alzheimer’s disease of about I confirmed case per second. This will quadruple
by 2040 and by then 70% of all cases will be living in developing and emerging
economies. These are average values and although a 100% increase can be
expected on average by 2040, this will be as high as 300% in China and India.
At present, the costs of Alzheimer’s disease to society in the EU is €160
billion and that would suggest, by extrapolation, a global cost in 2040, of €
1.6 trillion. This, in today’s terms is equivalent to the combined GDP of
Ireland, New Zealand, Israel, Singapore, Sweden and Nigeria. That’s a lot of
dosh and suffering by any measure.

For many years, researchers in nutrition have been interested
in studying the link between Alzheimer’s disease and dietary patters and the
two classes of nutrients of interest have been fats, specifically a protective
role for omega-3 fats and B-vitamins, specifically a protective role for folic
acid and vitamin B12. The data in this
area are strongly supported by epidemiological studies, which use blood markers
of these nutrients and the progression on dementia. However, as I pointed out
in a previous blog (“Brain food ~ get it early” 18th of June, 2012),
when dietary intervention studies are used to verify the associations found
between diet and dementia, the outcomes have been extremely disappointing and
this, I suggested may be due to a strong link between certain genetic factors,
diet and Alzheimer’s disease.

A recent paper published in the Proceedings of the National
Academy of Sciences[1]examines
the link between B-vitamin supplementation and the destruction of grey matter
material from those parts of the brain specifically associated with Alzheimer’s
disease. An initial study was carried out over two years with 156 subjects
(mean age of 77 years) with mild cognitive impairment. Half the group received
a placebo while the other got a B-vitamin supplement (folic acid, vitamin B12
and vitamin B6). The initial study showed that whereas brain size shrank in
both groups, B-vitamin group had, overall, a reduction in the rate of shrinkage
of grey matter. This paper now moves the same research from total brain
shrinkage to the loss of grey matter specifically in those regions of the brain
associated with Alzheimer’s disease (AD) In fact, the rate of shrinkage of
AD-sensitive grey matter was 3.7% in the placebo group compared to just 0.5% in
those receiving the B-vitamin supplement.

Homocysteine is a natural part of our blood biochemistry and
high levels of homocysteine have been associated with adverse health outcomes
and, classically, low levels of plasma folic acid and vitamin B-12 lead to high
level of blood homocysteine. In this study, the authors considered the effect
of B-vitamin supplementation on individuals with initially high or low levels
of plasma homocysteine. They found that if the levels of homocysteine were
elevated at the outset, the effects of B-vitamin supplementation was amplified
among individuals with elevated homocysteine (5.2% brain loss in the placebo
group with only 0.6% loss in the B-vitamin group).

This paper doesn’t use the usual “soft” end points used to
measure cognitive decline. Instead it used structural imaging techniques of
those regions of the brain sensitive to AD atrophy as an outcome measure. This
is a very interesting finding and even a strong indication that habitual high
intakes of certain B-vitamins will reduce the rate of neuro-degeneration from mild
cognitive impairment to AD, specifically, in those subjects with high plasma
homocysteine levels. However, it isn’t definitive proof of such a link. To
begin to build of a supporting body of evidence, one would need to prove that
accelerated (rate to be defined) shrinkage (extent to be defined) of AD
sensitive regions of the brain are indeed associated with the development of
Alzheimer’s disease in subject’s with specific biochemical (such as low
homocysteine levels on blood) and genetic (gene SNP’s to be determined)
attributes. Then we would have a robust biomarker. With that established then
all manner of dietary and drug interventions could be used to study their
outcome on the biomarker and, by implication Alzheimer’s disease itself.

One thing is sure. Alzheimer’s disease, like other
neurodegenerative diseases, is likely to have a significant nutritional
dimension.

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"Ever seen a fat fox ~ Human obesity explored"

About Me

I graduated from University College Dublin in 1971 with an Masters in Agricultural Chemistry, took a PhD at Sydney University in 1976 and joined the University of Southampton Medical School as a lecturer in human nutrition in 1977. In 1984 I returned to Ireland to take up a post at the Department of Clinical Medicine Trinity College Dublin and was appointed as professor of human nutrition. In 2006 I left Trinity and moved to University College Dublin as Director of the UCD Institute of Food and Health. I am a former President of the Nutrition Society and I've served on several EU and UN committees on nutrition and Health. I have published over 350+ peer reviewed scientific papers in Public Health Nutrition and Molecular Nutrition and am principal investigator on several national and EU projects (www.ucd.ie/jingo; www.food4me.org). My popular books are "Something to chew on ~ challenging controversies in human nutrition" and "Ever seen a fat fox: human obesity explored"